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Infectious Disease - Infective Esophagitis
FUNDAMENTAL DESCRIPTION
Esophageal infection caused by various fungus, viruses, and bacteria
EPIDEMIOLOGY Incidence
• Infectious esophagitis is uncommon in individuals with a normal immune system but prevalent among immunocompromised patients, those on medications that alter the normal esophageal microflora or immune function, and in cases where abnormalities impede the clearance of the esophageal lumen. • Primary cytomegalovirus (CMV) infections are prevalent in preschool children and young adults. Nonetheless, they infrequently induce esophagitis in immunocompetent individuals.
RISK FACTORS
• Immune deficiencies • Pharmacological agents that may modify immune function or esophageal microbiota • Anatomical anomalies or motility issues of the esophagus
GENERAL PREVENTION • Mitigation of risk factors, when feasible
• Suitable antiretroviral therapy to reduce immunosuppression in HIV-positive individuals
ETIOLOGY • The predominant etiological agents of infectious esophagitis in both immunocompromised and immunocompetent patients are one or a combination of the following three organisms: Candida spp., herpes simplex virus (HSV), and cytomegalovirus (CMV).
• The majority of Candida esophagitis cases are attributed to C. albicans. Diseases symptomatic of C. glabrata and C. krusei have also been documented.
• Other pathogens that may seldom induce infectious esophagitis include the following:
– Aspergillus species – Histoplasma species – Blastomyces dermatitidis – Varicella zoster virus
– Epstein–Barr virus – Human papillomavirus – Mycobacterium TB and Mycobacterium avium – Normal oropharyngeal flora (rarely) including Staphylococcus aureus, Staphylococcus epidermidis, Streptococcus viridans, and Bacillus species – Acute HIV infection
HISTORY OF DIAGNOSIS
Dysphagia, odynophagia, or both are the most prevalent symptoms.
• Chronic chest pain is also prevalent.
• Additional nonspecific clinical signs, such as weight loss, may arise from these symptoms or indicate an underlying illness responsible for the esophagitis.
Local problems, such as hemorrhage, esophageal perforation, or fistula formation, may arise in the presence of deep esophageal ulcerations caused by infected esophagitis.
Infectious esophagitis might be asymptomatic. The prevalence of asymptomatic esophageal infections is indeterminate.
PHYSICAL EXAMINATION
CMV esophagitis may manifest with systemic symptoms (e.g., fever, nausea, vomiting, or abdominal pain), while Candida and HSV esophagitis typically arise.
Oral lesions. Nonetheless, these sporadic discrepancies are not distinctive. The lack of thrush does not exclude the possibility of Candida esophagitis.
DIAGNOSTIC TESTS AND INTERPRETATION Laboratory
• Hematologic profile • Serological testing for HSV, CMV, and HIV • CMV antigenemia assays or CMV molecular amplification methods
• Brush cytology specimens acquired via endoscopy for the diagnosis of Candida and HSV esophagitis. • Tissue culture for the diagnosis of HSV and CMV esophagitis. Culture is not typically advised for diagnosing Candida esophagitis. This is designated for instances exhibiting clinical characteristics indicative of a pathogen resistant to conventional antifungal treatment.
Imaging
Radiographic assessment following a barium swallow reveals an uneven, frayed look of the esophagus mucosa in instances of Candida esophagitis. At times, the image is indistinguishable from that observed in instances of HSV and CMV esophagitis.
Diagnostic Procedures/Other • Endoscopy and tissue sampling for histological evaluation or brush cytology.
The standard endoscopic presentation of Candida esophagitis features white plaques on the mucosa that frequently hemorrhage upon removal by the endoscope.
Endoscopy in HSV esophagitis demonstrates tiny, well-defined ulcers with a yellowish base. The esophageal mucosa between lesions may frequently appear normal. Shallow, elongated ulcerations, encircled by seemingly normal mucosa, may characterize the endoscopic presentation of CMV esophagitis. Nevertheless, the endoscopic characteristics of Candida, HSV, or CMV esophagitis may be indistinguishable.
Pathological Observations
• Endoscopic tissue specimens may reveal: – Budding yeast cells, hyphae, or pseudohyphae in Candida esophagitis – Multinucleated giant cells and intranuclear inclusion bodies in HSV esophagitis – Cytomegaly of fibroblasts and endothelial cells with intranuclear and cytoplasmic inclusion bodies in
CMV esophagitis.
DIFFERENTIAL DIAGNOSIS
• Esophageal carcinoma (primary or metastatic). • Systemic conditions including: – Crohn's disease
Sarcoidosis
Collagen vascular disorders
Pill esophagitis may occur following the administration of specific antibiotics (such as tetracycline, doxycycline, clindamycin, ciprofloxacin, among others), potassium chloride, nonsteroidal anti-inflammatory medications, and quinidine.
Chemotherapy-induced esophagitis (dactinomycin, bleomycin, cytarabine, methotrexate, and other agents).
• Esophagitis resulting from radiation or the simultaneous application of radiation and chemotherapy.
• Inflammation resulting from sclerotherapy of esophageal varices.
• Idiopathic (aphthous) esophageal ulcers associated with HIV infection.
Oral lesions are frequently observed in patients with Candida and HSV esophagitis, although CMV esophagitis is infrequently linked to stomatitis.
INITIAL THERAPY MEDICATION
Systemic antifungal therapy is invariably necessary for Candida esophagitis (A-II).
A diagnostic trial of antifungal medication is warranted prior to doing an endoscopic examination (B-II).
Oral fluconazole at a dosage of 200–400 mg (3–6 mg/kg) daily for a duration of 14–21 days is advised (A-I). For individuals unable to endure oral therapy: Administer intravenous fluconazole 400 mg (6 mg/kg) daily, deoxycholate amphotericin B 0.3–0.7 mg/kg daily, or an echinocandin (B-II).
For fluconazole-refractory disease: Itraconazole solution 200 mg daily, posaconazole suspension 400 mg twice daily, or voriconazole 200 mg twice daily, taken intravenously or orally for 14–21 days.
• For recurring infections: Administer suppressive therapy with fluconazole at a dosage of 100–200 mg three times weekly (3) (A-I).
• In individuals with AIDS, the use of HAART is advised to mitigate recurring infections (A-I).
HSV esophagitis typically resolves spontaneously in immunocompetent individuals.
Immunocompromised people ought to receive antiviral medications for a duration of 14 to 21 days. Acyclovir 400 mg orally five times daily, valacyclovir 1 g orally three times daily, famciclovir 500 mg orally three times daily. For individuals unable to endure oral therapy: Acyclovir 5 mg/kg intravenously every 8 hours for 7 to 14 days, succeeded by an oral antiviral for a minimum of 1 further week.
Prophylactic therapy with acyclovir at a dosage of 200–400 mg orally per day or 5 mg/kg intravenously twice day may be warranted in cases with elevated risk for HSV reactivation.
CMV esophagitis is managed with ganciclovir at a dosage of 5 mg/kg intravenously twice day for a minimum duration of 2 weeks.
Maintenance therapy with valganciclovir 900 mg orally daily may be required to prevent recurrence of CMV esophagitis in individuals with significant immunocompromise.
To avert CMV infection, CMV seronegative transplant recipients from seropositive donors should undergo antiviral prophylaxis.
Idiopathic (aphthous) esophageal ulcers in HIV infection are managed with prednisone or thalidomide.
Second Line
• For fluconazole-refractory Candida esophagitis: Micafungin 150 mg daily, caspofungin 50 mg daily, anidulafungin 200 mg daily, or deoxycholate
Amphotericin B 0.3–0.7 mg/kg per day (B-II).
• Echinocandins correlate with elevated relapse rates in comparison to fluconazole. • For ganciclovir-resistant HSV or CMV esophagitis: Foscarnet.
INPATIENT CONSIDERATIONS
Criteria for Admission
Outpatient care is suitable unless the patient's immune state is significantly weakened or the infection is exceedingly severe. In such instances, hospitalization may be required.
Intravenous Fluids
Should the patient endure significant odynophagia or if esophagitis is coupled with oral lesions that hinder chewing or swallowing, the provision of intravenous fluids may be requisite.
CONTINUING MANAGEMENT POST-TREATMENT SUGGESTIONS
The anticipated course and prognosis are contingent upon the underlying disease and pathogen; in cases of severe immunosuppression, extended therapy with efficacious drugs is required.
• Patients diagnosed with infectious esophagitis should schedule a follow-up appointment two weeks post-symptom resolution. • The majority of patients with Candida esophagitis typically experience symptom clearance within seven days of initiating treatment.
Myelosuppression is the primary adverse effect of ganciclovir therapy. The simultaneous use of zidovudine may exacerbate myelosuppression.
COMPLICATIONS
• Complications are rare. Severe local consequences may arise from deep esophageal ulcers, including massive hemorrhage.
– Esophageal perforation – Esophagobronchial or esophagomediastinal fistulas
FUNDAMENTAL DESCRIPTION
Esophageal infection caused by various fungus, viruses, and bacteria
EPIDEMIOLOGY Incidence
• Infectious esophagitis is uncommon in individuals with a normal immune system but prevalent among immunocompromised patients, those on medications that alter the normal esophageal microflora or immune function, and in cases where abnormalities impede the clearance of the esophageal lumen. • Primary cytomegalovirus (CMV) infections are prevalent in preschool children and young adults. Nonetheless, they infrequently induce esophagitis in immunocompetent individuals.
RISK FACTORS
• Immune deficiencies • Pharmacological agents that may modify immune function or esophageal microbiota • Anatomical anomalies or motility issues of the esophagus
GENERAL PREVENTION • Mitigation of risk factors, when feasible
• Suitable antiretroviral therapy to reduce immunosuppression in HIV-positive individuals
ETIOLOGY • The predominant etiological agents of infectious esophagitis in both immunocompromised and immunocompetent patients are one or a combination of the following three organisms: Candida spp., herpes simplex virus (HSV), and cytomegalovirus (CMV).
• The majority of Candida esophagitis cases are attributed to C. albicans. Diseases symptomatic of C. glabrata and C. krusei have also been documented.
• Other pathogens that may seldom induce infectious esophagitis include the following:
– Aspergillus species – Histoplasma species – Blastomyces dermatitidis – Varicella zoster virus
– Epstein–Barr virus – Human papillomavirus – Mycobacterium TB and Mycobacterium avium – Normal oropharyngeal flora (rarely) including Staphylococcus aureus, Staphylococcus epidermidis, Streptococcus viridans, and Bacillus species – Acute HIV infection
HISTORY OF DIAGNOSIS
Dysphagia, odynophagia, or both are the most prevalent symptoms.
• Chronic chest pain is also prevalent.
• Additional nonspecific clinical signs, such as weight loss, may arise from these symptoms or indicate an underlying illness responsible for the esophagitis.
Local problems, such as hemorrhage, esophageal perforation, or fistula formation, may arise in the presence of deep esophageal ulcerations caused by infected esophagitis.
Infectious esophagitis might be asymptomatic. The prevalence of asymptomatic esophageal infections is indeterminate.
PHYSICAL EXAMINATION
CMV esophagitis may manifest with systemic symptoms (e.g., fever, nausea, vomiting, or abdominal pain), while Candida and HSV esophagitis typically arise.
Oral lesions. Nonetheless, these sporadic discrepancies are not distinctive. The lack of thrush does not exclude the possibility of Candida esophagitis.
DIAGNOSTIC TESTS AND INTERPRETATION Laboratory
• Hematologic profile • Serological testing for HSV, CMV, and HIV • CMV antigenemia assays or CMV molecular amplification methods
• Brush cytology specimens acquired via endoscopy for the diagnosis of Candida and HSV esophagitis. • Tissue culture for the diagnosis of HSV and CMV esophagitis. Culture is not typically advised for diagnosing Candida esophagitis. This is designated for instances exhibiting clinical characteristics indicative of a pathogen resistant to conventional antifungal treatment.
Imaging
Radiographic assessment following a barium swallow reveals an uneven, frayed look of the esophagus mucosa in instances of Candida esophagitis. At times, the image is indistinguishable from that observed in instances of HSV and CMV esophagitis.
Diagnostic Procedures/Other • Endoscopy and tissue sampling for histological evaluation or brush cytology.
The standard endoscopic presentation of Candida esophagitis features white plaques on the mucosa that frequently hemorrhage upon removal by the endoscope.
Endoscopy in HSV esophagitis demonstrates tiny, well-defined ulcers with a yellowish base. The esophageal mucosa between lesions may frequently appear normal. Shallow, elongated ulcerations, encircled by seemingly normal mucosa, may characterize the endoscopic presentation of CMV esophagitis. Nevertheless, the endoscopic characteristics of Candida, HSV, or CMV esophagitis may be indistinguishable.
Pathological Observations
• Endoscopic tissue specimens may reveal: – Budding yeast cells, hyphae, or pseudohyphae in Candida esophagitis – Multinucleated giant cells and intranuclear inclusion bodies in HSV esophagitis – Cytomegaly of fibroblasts and endothelial cells with intranuclear and cytoplasmic inclusion bodies in
CMV esophagitis.
DIFFERENTIAL DIAGNOSIS
• Esophageal carcinoma (primary or metastatic). • Systemic conditions including: – Crohn's disease
Sarcoidosis
Collagen vascular disorders
Pill esophagitis may occur following the administration of specific antibiotics (such as tetracycline, doxycycline, clindamycin, ciprofloxacin, among others), potassium chloride, nonsteroidal anti-inflammatory medications, and quinidine.
Chemotherapy-induced esophagitis (dactinomycin, bleomycin, cytarabine, methotrexate, and other agents).
• Esophagitis resulting from radiation or the simultaneous application of radiation and chemotherapy.
• Inflammation resulting from sclerotherapy of esophageal varices.
• Idiopathic (aphthous) esophageal ulcers associated with HIV infection.
Oral lesions are frequently observed in patients with Candida and HSV esophagitis, although CMV esophagitis is infrequently linked to stomatitis.
INITIAL THERAPY MEDICATION
Systemic antifungal therapy is invariably necessary for Candida esophagitis (A-II).
A diagnostic trial of antifungal medication is warranted prior to doing an endoscopic examination (B-II).
Oral fluconazole at a dosage of 200–400 mg (3–6 mg/kg) daily for a duration of 14–21 days is advised (A-I). For individuals unable to endure oral therapy: Administer intravenous fluconazole 400 mg (6 mg/kg) daily, deoxycholate amphotericin B 0.3–0.7 mg/kg daily, or an echinocandin (B-II).
For fluconazole-refractory disease: Itraconazole solution 200 mg daily, posaconazole suspension 400 mg twice daily, or voriconazole 200 mg twice daily, taken intravenously or orally for 14–21 days.
• For recurring infections: Administer suppressive therapy with fluconazole at a dosage of 100–200 mg three times weekly (3) (A-I).
• In individuals with AIDS, the use of HAART is advised to mitigate recurring infections (A-I).
HSV esophagitis typically resolves spontaneously in immunocompetent individuals.
Immunocompromised people ought to receive antiviral medications for a duration of 14 to 21 days. Acyclovir 400 mg orally five times daily, valacyclovir 1 g orally three times daily, famciclovir 500 mg orally three times daily. For individuals unable to endure oral therapy: Acyclovir 5 mg/kg intravenously every 8 hours for 7 to 14 days, succeeded by an oral antiviral for a minimum of 1 further week.
Prophylactic therapy with acyclovir at a dosage of 200–400 mg orally per day or 5 mg/kg intravenously twice day may be warranted in cases with elevated risk for HSV reactivation.
CMV esophagitis is managed with ganciclovir at a dosage of 5 mg/kg intravenously twice day for a minimum duration of 2 weeks.
Maintenance therapy with valganciclovir 900 mg orally daily may be required to prevent recurrence of CMV esophagitis in individuals with significant immunocompromise.
To avert CMV infection, CMV seronegative transplant recipients from seropositive donors should undergo antiviral prophylaxis.
Idiopathic (aphthous) esophageal ulcers in HIV infection are managed with prednisone or thalidomide.
Second Line
• For fluconazole-refractory Candida esophagitis: Micafungin 150 mg daily, caspofungin 50 mg daily, anidulafungin 200 mg daily, or deoxycholate
Amphotericin B 0.3–0.7 mg/kg per day (B-II).
• Echinocandins correlate with elevated relapse rates in comparison to fluconazole. • For ganciclovir-resistant HSV or CMV esophagitis: Foscarnet.
INPATIENT CONSIDERATIONS
Criteria for Admission
Outpatient care is suitable unless the patient's immune state is significantly weakened or the infection is exceedingly severe. In such instances, hospitalization may be required.
Intravenous Fluids
Should the patient endure significant odynophagia or if esophagitis is coupled with oral lesions that hinder chewing or swallowing, the provision of intravenous fluids may be requisite.
CONTINUING MANAGEMENT POST-TREATMENT SUGGESTIONS
The anticipated course and prognosis are contingent upon the underlying disease and pathogen; in cases of severe immunosuppression, extended therapy with efficacious drugs is required.
• Patients diagnosed with infectious esophagitis should schedule a follow-up appointment two weeks post-symptom resolution. • The majority of patients with Candida esophagitis typically experience symptom clearance within seven days of initiating treatment.
Myelosuppression is the primary adverse effect of ganciclovir therapy. The simultaneous use of zidovudine may exacerbate myelosuppression.
COMPLICATIONS
• Complications are rare. Severe local consequences may arise from deep esophageal ulcers, including massive hemorrhage.
– Esophageal perforation – Esophagobronchial or esophagomediastinal fistulas
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